Archive for the ‘Psoriasis’ Category

Ted Barrus, an ordinary guy from Pullman, Wash., calls himself an idiot -- more specifically, a "fire-breathing idiot."

Barrus, 37, doesn't actually breathe fire, but his main hobby is sampling extremely hot peppers that make his mouth seem as if it's on fire. His latest sampling is the Trinidad Moruga Scorpion, the pepper recently named world's hottest by researchers at the New Mexico State University's Chile Pepper Institute.

"I do this to bring chilies and the fun they can be to the masses," Barrus said, who regularly posts videos of his reactions on YouTube.

Barrus passes on jalapenos, and even habaneros, and opts only for the peppers known as "superhots" and "nuclears," such as the Trinidad Moruga Scorpion. This "superhot" hit an average of more than 1.2 million Scoville heat units, making it many thousand times hotter than the jalapeno, which hits about 5,000 units.

Scoville units measure the amount of spicy heat in chili peppers based on the amount of capsaicin, a compound that makes the peppers, well, hot.

So far, Barrus has dared to eat six of these mouth-on-fire peppers, including four in one sitting, which he says is "the most difficult challenge I have ever done."

As in several of his earlier pepper-sampling videos, seconds after he bites into the Trinidad Moruga Scorpion, Barrus' face turns red, his eyes water and he starts to grimace and groan.

Despite the incredibly intense burning -- which persists for about 20 minutes -- Barrus says the 40-minute period of bliss that follows is worth the pain.

"There's a massive endorphin rush, and I feel really good after all the pain and craziness," he said. "My body starts tingling all over, my hands and arms start to go numb, and I sometimes get lightheaded and euphoric. It feels good." Released in response to stress and pain, endorphins are brain chemicals that reduce the perception of pain.

And it's exactly that endorphin rush that makes capsaicin an effective remedy for pain and other medical conditions, researchers say.

"The endorphins work to block the heat. The body produces them in response to the heat, which it senses as pain," said Paul Bosland, co-founder and director of New Mexico State University's Chile Pepper Institute.

"It's used for all kinds of arthritis pain, as well as for neuropathic pain and dermatologic conditions that have a painful itch," said Dr. Ashwin Mehta, director of integrative medicine at the University of Miami's Miller School of Medicine.

Capsaicin is also used by people with the skin disease psoriasis to decrease itching and inflammation, according to the university.

Some research has also suggested that capsaicin can also help with appetite suppression, but there are not yet any solid data to determine what role, if any, the chemical plays in weight loss.

Studies have also suggested that capsaicin may play help kill off prostate cancer cells.

"In test tubes, researchers found a correlation betwen increased cell death and capsaicin," said Mehta.

There have also been studies that found that people who eat a lot of chili peppers have a lower incidence of prostate cancer, Bosland said.

"This doesn't mean hot peppers cure prostate cancer, but it may play a role in preventing it," he said. "It has nothing to do with the heat per se, but they have a lot of carotenoids and flavonoids, which scavenge free radicals in our system, and free radicals are known to cause cancer."

According to the University of Maryland Medical Center, capsaicin, provided it's in an extremely diluted form, can also be used to treat ear infections. Additionally, one study found that the compound may help treat heartburn. More research is needed to examine that relationship further, and studies are also under way to determine its effects on certain cardiovascular conditions.

But because it's so hot -- pure capsaicin extract is rated at more than 15 million Scoville units -- the compound should be used only as directed by a physician, and in moderation.

And Barrus also encourages people not accustomed to eating hot peppers to take the heat warnings seriously.

"These peppers are not for the average Joe. They're for idiots like me," he said, joking.

Eczema is a type of atopic dermatitis that results in red, irritated skin that may ooze and crust over causing the skin to appear scaly, according to the Australasian College of Dermatologists. Eczema of the fingernails occurs under and around the nail beds and occurs when the skin becomes irritated or is exposed to chronic moisture, such as when a child repeatedly sucks his thumb. There are several ways to treat nail eczema to clear up the unwanted redness and irritation.

Moisturizing lotion

Cold compress

Avoid over-exposure to water. This means staying out of the pool for extended periods of time and wearing rubber gloves when cleaning and doing the dishes. This will cut down on the dryness that will make nail eczema worse.

Apply moisturizing lotion to the nail beds at least once a day. This will keep the skin supple and can be used to treat eczema all over your body to help seal in moisture.

Identify what triggers your eczema and attempt to avoid it. According to Mayo Clinic.com, common eczema triggers include stress, contact with certain household cleaners, sweating and harsh soaps and perfumes.

Place a cold compress on the affected finger or toe nails when a flare-up is occurring. This could include a bag of peas wrapped in a hand towel or an ice pack. This will relieve the irritation, redness and swelling that is associated with eczema.

Cover the nails with a one percent hydrocortisone cream. This will help relieve any itching that might accompany eczema.

Speak to your doctor about any medications that will help treat the symptoms of nail eczema. These include immunomodulators that, according to the Mayo Clinic, will lessen the effects the immune system has on eczema. Another medication that may be prescribed is prednisone, which is a steroid that will reduce the inflammation of eczema.

Eczema and psoriasis are often mistaken for each other because they tend to share similar symptoms. ... Nail changes do occur with...

It is possible that you have lichen planus, psoriasis or eczema, ... Fingernails provide a degree of protection to the soft, sensitive...

Whether you have thick toenails because of a skin condition such as eczema or psoriasis, fungus or even injury, simple alternatives to...

Eczema is a condition that results in itchy, inflamed skin. It is a chronic irritating rash occurring in flareups. It generally runs...

Most commonly, white spots are caused by trauma to the nail, similar to a bruise on your skin. ... or skin conditions...

What is psoriasis? Watch this video as dermatologist David M. Pariser, MD, FAAD, explains why we get psoriasis and the benefits of treatment.

To watch the entire video, which includes inspiring tips from Jerry Mathers, who lives with psoriasis and is best known as the Beaver in the TV show "Leave it to Beaver," visit thePsoriasis video library.

Psoriasis (sore-EYE-ah-sis) is a chronic (long-lasting) disease. It develops when a persons immune system sends faulty signals that tell skin cells to grow too quickly. New skin cells form in days rather than weeks.

The body does not shed these excess skin cells. The skin cells pile up on the surface of the skin, causing patches of psoriasis to appear. Psoriasis may look contagious, but it's not.

You cannot get psoriasis from touching someone who has it. To get psoriasis, a person must inherit the genes that cause it.

If you have psoriasis, you will have one or more of these types:

Some people get more than one type. Sometimes a person gets one type of psoriasis, and then the type of psoriasis changes.

Image used with permission of the American Academy of Dermatology National Library of Dermatologic Teaching Slides.

Psoriasis is a chronic inflammatory skin condition characterised by clearly defined, red and scaly plaques (thickened skin). It is classified into several subtypes.

Psoriasis affects 24% of males and females. It can start at any age including childhood, with peaks of onset at 1525 years and 5060 years. It tends to persist lifelong, fluctuating in extent and severity. It is particularly common in Caucasians, but may affect people of any race. About one third of patients have family members with psoriasis.

Psoriasis usually presents with symmetrically distributed, red, scaly plaques with well-defined edges. The scale is typically silvery white, except in skin folds where the plaques often appear shiny and they may have a moist peeling surface. The most common sites are scalp, elbows and knees, but any part of the skin can be involved. The plaques are usually very persistent without treatment.

Itch is mostly mild but may be severe in some patients, leading to scratching and lichenification (thickened leathery skin with increased skin markings). Painful skin cracks or fissures may occur.

When psoriatic plaques clear up, they may leave brown or pale marks that can be expected to fade over several months.

Certain features of psoriasis can be categorised to help determine appropriate investigations and treatment pathways. Overlap may occur.

Generalised pustulosis and localised palmoplantar pustulosis are no longer classified within the psoriasis spectrum.

Patients with psoriasis are more likely than other people to have other health conditions listed here.

Psoriasis is multifactorial. It is classified as an immune-mediated inflammatory disease (IMID).

Genetic factors are important. An individual's genetic profile influences their type of psoriasis and its response to treatment.

Theories about the causes of psoriasis need to explain why the skin is red, inflamed and thickened. It is clear that immune factors and inflammatory cytokines (messenger proteins) such is IL1 and TNF are responsible for the clinical features of psoriasis. Current theories are exploring the TH17 pathway and release of the cytokine IL17A.

Psoriasis is diagnosed by its clinical features. If necessary, diagnosis is supported by typical skin biopsy findings.

Medical assessment entails a careful history, examination, questioning about effect of psoriasis on daily life, and evaluation of comorbid factors.

Validated tools used to evaluate psoriasis include:

The severity of psoriasis is classified as mild in 60% of patients, moderate in 30% and severe in 10%.

Evaluation of comorbidities may include:

Patients with psoriasis should ensure they are well informed about their skin condition and its treatment. There are benefits from not smoking, avoiding excessive alcohol and maintaining optimal weight.

Mild psoriasis is generally treated with topical agents alone. Which treatment is selected may depend on body site, extent and severity of the psoriasis.

Moderate to severe psoriasis warrants treatment with a systemic agent and/or phototherapy. The most common treatments are:

Other medicines occasionally used for psoriasis include:

Most psoriasis centres offer phototherapy with ultraviolet (UV) radiation, often in combination with topical or systemic agents. Types of phototherapy include

Biologics or targeted therapies are reserved for conventional treatment-resistant severe psoriasis, mainly because of expense, as side effects compare favourably with other systemic agents. These include:

STELARA is a prescription medicine approved to treat adults 18 years and older with moderate or severe plaque psoriasis that involves large areas or many areas of their body, who may benefit from taking injections or pills (systemic therapy) or phototherapy (treatment using ultraviolet light alone or with pills).

STELARA is a prescription medicine approved to treat adults 18 years and older with active psoriatic arthritis, either alone or with methotrexate.

STELARA is a 45 mg or 90 mg injection given under the skin as directed by your doctor at weeks 0, 4, and every 12 weeks thereafter. It is administered by a healthcare provider or self-injected only after proper training.

STELARA can make you more likely to get infections or make an infection that you have worse. People who have a genetic problem where the body does not make any of the proteins interleukin 12 (IL-12)Proteins that increase the growth and function of white blood cells, which are found in your immune system. and interleukin 23 (IL-23)Proteins that increase the growth and function of white blood cells, which are found in your immune system. are at a higher risk for certain serious infections that can spread throughout the body and cause death. It is not known if people who take STELARA will get any of these infections because of the effects of STELARA on these proteins.

Cancers

STELARA may decrease the activity of your immune systemA system inside the body that protects against germs and infections. and increase your risk for certain types of cancer. Tell your doctor if you have ever had any type of cancer. Some people who had risk factors for skin cancer developed certain types of skin cancers while receiving STELARA. Tell your doctor if you have any new skin growths.

Reversible posterior leukoencephalopathy syndrome (RPLS)

RPLS is a rare condition that affects the brain and can cause death. The cause of RPLS is not known. If RPLS is found early and treated, most people recover. Tell your doctor right away if you have any new or worsening medical problems including: headache, seizures, confusion, and vision problems.

Serious Allergic Reactions

Serious allergic reactions can occur. Get medical help right away if you have any symptoms such as: feeling faint, swelling of your face, eyelids, tongue, or throat, trouble breathing, throat or chest tightness, or skin rash.

Before receiving STELARA, tell your doctor if you:

When prescribed STELARA:

You are encouraged to report negative side effects of prescription drugs to the FDA. Visit http://www.fda.gov/medwatch or call 1-800-FDA-1088.

Please read the Full Prescribing Information, including the Medication Guide for STELARA, and discuss any questions you have with your doctor.

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Psoriasis Journey

Regardless of severity, patients with the often disfiguring skin condition psoriasis face an elevated risk for depression, new research suggests.

By Steven ReinbergHealthDay Reporter WEDNESDAY, Sept. 30, 2015 (HealthDay News) Two experimental drugs show promise in treating psoriasis and a related condition, psoriatic arthritis, new studies report. The drugs, brodalumab and secukinumab (Cosentyx), represent a new approach to treatment, said Michael Siegel, director of research programs at the National Psoriasis Foundation. These studies show how targeting [...]

People with psoriasis may be twice as likely to experience depression as those without the common skin condition, regardless of its severity, a new study suggests.

By Steven ReinbergHealthDay Reporter WEDNESDAY, July 8, 2015 (HealthDay News) Preliminary trial results suggest that an experimental psoriasis drug may control the chronic skin disease better than the current standard treatment. The drug, guselkumab, was compared to the commonly used medication adalimumab (Humira, Enbrel) in a study involving nearly 300 patients with plaque psoriasis. Up to 86 [...]

TUESDAY, June 16, 2015 (HealthDay News) Many patients with the skin disease psoriasis showed significant improvement when taking an experimental drug called ixekizumab, according to a late-stage, phase 3 clinical trial. The visible effects of psoriasis can have a major and life-ruining impact on peoples confidence and self-esteem, study leader Chris Griffiths, a professor of [...]

Psoriasis is a long-lasting autoimmune disease characterized by patches of abnormal skin.[1] These skin patches are typically red, itchy, and scaly. They may vary in severity from small and localized to complete body coverage.[2] Injury to the skin can trigger psoriatic skin changes at that spot, which is known as Koebner phenomenon.[3]

There are five main types of psoriasis: plaque, guttate, inverse, pustular, and erythrodermic.[1] Plaque psoriasis, also known as psoriasis vulgaris, makes up about 90% of cases. It typically presents with red patches with white scales on top. Areas of the body most commonly affected are the back of the forearms, shins, around the belly button, and the scalp.[4] Guttate psoriasis has drop shapped lesions.[1] Pustular psoriasis presents with small non-infectious pus filled blisters.[5] Inverse psoriasis forms red patches in skin folds.[1] Erythrodermic psoriasis occurs when the rash becomes very widespread, and can develop from any of the other types. Fingernails and toenails are affected in most people at some point in time. This may include pits in the nails or changes in nail color.[4]

Psoriasis is generally thought to be a genetic disease which is triggered by environmental factors.[2] In twin studies, identical twins are three times more likely to both be affected compared to non-identical twins; this suggests that shared genetic risk factors predispose to psoriasis. Symptoms often worsen during winter and with certain medications such as beta blockers or NSAIDs.[4] Infections and psychological stress may also play a role.[1][2] Psoriasis is not contagious. The underlying mechanism involves the immune system reacting to skin cells. Diagnosis is typically based on the signs and symptoms.[4]

There is no cure for psoriasis. However, various treatments can help control the symptoms.[4] These treatments may include steroid creams, vitamin D3 cream, ultraviolet light, and immune system suppressing medications such as methotrexate.[1] About 75% of people can be managed with creams alone.[4] The disease affects 24% of the population.[6] Both males and females are affected with equal frequency.[1] Psoriasis is associated with an increased risk of psoriatic arthritis, lymphomas, cardiovascular disease, Crohn's disease, and depression.[4] Psoriatic arthritis affects up to 30% of individuals with psoriasis.[5]

Psoriasis vulgaris (also known as chronic stationary psoriasis or plaque-like psoriasis) is the most common form and affects 85%90% of people with psoriasis.[7] Plaque psoriasis typically appears as raised areas of inflamed skin covered with silvery-white scaly skin. These areas are called plaques and are most commonly found on the elbows, knees, scalp, and back.[7][8]Psoriatic erythroderma (erythrodermic psoriasis) involves widespread inflammation and exfoliation of the skin over most of the body surface. It may be accompanied by severe itching, swelling, and pain. It is often the result of an exacerbation of unstable plaque psoriasis, particularly following the abrupt withdrawal of systemic glucocorticoids.[9] This form of psoriasis can be fatal as the extreme inflammation and exfoliation disrupt the body's ability to regulate temperature and perform barrier functions.[10]

A person's arm covered with plaque psoriasis

Pustular psoriasis appears as raised bumps filled with noninfectious pus (pustules).[11] The skin under and surrounding the pustules is red and tender.[12] Pustular psoriasis can be localized, commonly to the hands and feet (palmoplantar pustulosis), or generalized with widespread patches occurring randomly on any part of the body. Acrodermatitis continua is a form of localized psoriasis limited to the fingers and toes that may spread to the hands and feet.[12]Pustulosis palmaris et plantaris is another form of localized pustular psoriasis similar to acrodermatitis continua with pustules erupting from red, tender, scaly skin found on the palms of the hands and the soles of the feet.[12]

Generalized pustular psoriasis (pustular psoriasis of von Zumbusch), also known as impetigo herpetiformis during pregnancy,[13] is a rare and severe form of psoriasis that may require hospitalization. The development of generalized pustular psoriasis is often caused by an infection, abrupt withdrawal of topical corticosteroid treatment, pregnancy, hypocalcemia, medications, or following an irritating topical treatment for plaque psoriasis.[12] This form of psoriasis is characterized by an acute onset of numerous pustules on top of tender red skin. This skin eruption is often accompanied by a fever, muscle aches, nausea, and an elevated white blood cell count.[12]Annular pustular psoriasis (APP), a rare form of generalized pustular psoriasis, is the most common type seen during childhood.[13] APP tends to occur in women more frequently than in men, and is usually less severe than other forms of generalized pustular psoriasis such as impetigo herpetiformis.[13] This form of psoriasis is characterized by ring-shaped plaques with pustules around the edges and yellow crusting.[13] APP most often affects the torso, neck, arms, and legs.[13]

Inverse psoriasis (also known as flexural psoriasis) appears as smooth, inflamed patches of skin. The patches frequently affect skin folds, particularly around the genitals (between the thigh and groin), the armpits, in the skin folds of an overweight abdomen (known as panniculus), between the buttocks in the intergluteal cleft, and under the breasts in the inframammary fold. Heat, trauma, and infection are thought to play a role in the development of this atypical form of psoriasis.[15]Napkin psoriasis is a subtype of psoriasis common in infants characterized by red papules with silver scale in the diaper area that may extend to the torso or limbs.[16] Napkin psoriasis is often misdiagnosed as napkin dermatitis.[17]

Guttate psoriasis is characterized by numerous small, scaly, red or pink, droplet-like lesions (papules). These numerous spots of psoriasis appear over large areas of the body, primarily the trunk, but also the limbs and scalp. Guttate psoriasis is often triggered by a streptococcal infection, typically streptococcal pharyngitis.[15] The reverse is not true.

Oral psoriasis is very rare,[18] in contrast to lichen planus, another common papulosquamous disorder that commonly involves both the skin and mouth. When psoriasis involves the oral mucosa (the lining of the mouth), it may be asymptomatic,[18] but it may appear as white or grey-yellow plaques.[18]Fissured tongue is the most common finding in those with oral psoriasis and has been reported to occur in 6.5-20% of people with psoriasis affecting the skin. The microscopic appearance of oral mucosa affected by geographic tongue (migratory stomatitis) is very similar to the appearance of psoriasis.[19] However, modern studies have failed to demonstrate any link between the two conditions.[20]

Seborrheic-like psoriasis is a common form of psoriasis with clinical aspects of psoriasis and seborrheic dermatitis, and may be difficult to distinguish from the latter. This form of psoriasis typically manifests as red plaques with greasy scales in areas of higher sebum production such as the scalp, forehead, skin folds next to the nose, skin surrounding the mouth, skin on the chest above the sternum, and in skin folds.[16]

Psoriatic arthritis is a form of chronic inflammatory arthritis that has a highly variable clinical presentation and frequently occurs in association with skin and nail psoriasis.[21][22] It typically involves painful inflammation of the joints and surrounding connective tissue and can occur in any joint, but most commonly affects the joints of the fingers and toes. This can result in a sausage-shaped swelling of the fingers and toes known as dactylitis.[21] Psoriatic arthritis can also affect the hips, knees, spine (spondylitis), and sacroiliac joint (sacroiliitis).[23] About 30% of individuals with psoriasis will develop psoriatic arthritis.[7] Skin manifestations of psoriasis tend to occur before arthritic manifestations in about 75% of cases.[22]

Psoriasis can affect the nails and produces a variety of changes in the appearance of finger and toe nails. Nail psoriasis occurs in 40-45% of people with psoriasis affecting the skin and has a lifetime incidence of 80-90% in those with psoriatic arthritis.[24] These changes include pitting of the nails (pinhead-sized depressions in the nail is seen in 70% with nail psoriasis), whitening of the nail, small areas of bleeding from capillaries under the nail, yellow-reddish discoloration of the nails known as the oil drop or salmon spot, thickening of the skin under the nail (subungual hyperkeratosis), loosening and separation of the nail (onycholysis), and crumbling of the nail.[24]

In addition to the appearance and distribution of the rash, specific medical signs may be used by medical practitioners to assist with diagnosis. These may include Auspitz's sign (pinpoint bleeding when scale is removed), Koebner phenomenon (psoriatic skin lesions induced by trauma to the skin),[16] and itching and pain localized to papules and plaques.[15][16]

The cause of psoriasis is not fully understood, but a number of theories exist.

Around one-third of people with psoriasis report a family history of the disease, and researchers have identified genetic loci associated with the condition. Identical twin studies suggest a 70% chance of a twin developing psoriasis if the other twin has the disorder. The risk is around 20% for nonidentical twins. These findings suggest both a genetic susceptibility and an environmental response in developing psoriasis.[25]

Psoriasis has a strong hereditary component, and many genes are associated with it, but it is unclear how those genes work together. Most of the identified genes relate to the immune system, particularly the major histocompatibility complex (MHC) and T cells. Genetic studies are valuable due to their ability to identify molecular mechanisms and pathways for further study and potential drug targets.[26]

Classic genome-wide linkage analysis has identified nine loci on different chromosomes associated with psoriasis. They are called psoriasis susceptibility 1 through 9 (PSORS1 through PSORS9). Within those loci are genes on pathways that lead to inflammation. Certain variations (mutations) of those genes are commonly found in psoriasis.[26]Genome-wide association scans have identified other genes that are altered to characteristic variants in psoriasis. Some of these genes express inflammatory signal proteins, which affect cells in the immune system that are also involved in psoriasis. Some of these genes are also involved in other autoimmune diseases.[26]

The major determinant is PSORS1, which probably accounts for 35%50% of psoriasis heritability. It controls genes that affect the immune system or encode skin proteins that are overabundant with psoriasis. PSORS1 is located on chromosome 6 in the major histocompatibility complex (MHC), which controls important immune functions. Three genes in the PSORS1 locus have a strong association with psoriasis vulgaris: HLA-C variant HLA-Cw6,[27] which encodes a MHC class I protein; CCHCR1, variant WWC, which encodes a coiled protein that is overexpressed in psoriatic epidermis; and CDSN, variant allele 5, which encodes corneodesmosin, a protein which is expressed in the granular and cornified layers of the epidermis and upregulated in psoriasis.[26]

Two major immune system genes under investigation are interleukin-12 subunit beta (IL12B) on chromosome 5q, which expresses interleukin-12B; and IL23R on chromosome 1p, which expresses the interleukin-23 receptor, and is involved in T cell differentiation. Interleukin-23 receptor and IL12B have both been strongly linked with psoriasis.[27] T cells are involved in the inflammatory process that leads to psoriasis.[26] These genes are on the pathway that up-regulate tumor necrosis factor- and nuclear factor B, two genes involved in inflammation.[26] Recently, the first gene directly linked to psoriasis has been identified. A rare mutation in the gene encoding for the CARD14 protein plus an environmental trigger was enough to cause plaque psoriasis (the most common form of psoriasis).[28][29]

Conditions reported as accompanying a worsening of the disease include chronic infections, stress, and changes in season and climate.[27] Others include hot water, scratching psoriasis skin lesions, skin dryness, excessive alcohol consumption, cigarette smoking, and obesity.[27][30][31]

People with advanced HIV/AIDS often exhibit psoriasis.[32] The rate of psoriasis in HIV-positive individuals is comparable to that of HIV-negative individuals, however, psoriasis tends to be more severe in people infected with HIV.[33] A much higher rate of psoriatic arthritis occurs in HIV-positive individuals with psoriasis than in those without the infection.[33] The immune response in those infected with HIV is typically characterized by cellular signals from Th2 subset of CD4+ helper T cells,[32] whereas the immune response in psoriasis vulgaris is characterized by a pattern of cellular signals typical of Th1 subset of CD4+ helper T cells and Th17 helper T cells.[34][35] It is hypothesized that the diminished CD4+-T cell presence causes an overactivation of CD8+-T cells, which are responsible for the exacerbation of psoriasis in HIV-positive people. Psoriasis in those with HIV/AIDS is often severe and may be untreatable with conventional therapy.[36]

Psoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin.[39] Abnormal production of skin cells (especially during wound repair) and an overabundance of skin cells result from the sequence of pathological events in psoriasis.[12] Skin cells are replaced every 35 days in psoriasis rather than the usual 2830 days.[40] These changes are believed to stem from the premature maturation of keratinocytes induced by an inflammatory cascade in the dermis involving dendritic cells, macrophages, and T cells (three subtypes of white blood cells).[7][33] These immune cells move from the dermis to the epidermis and secrete inflammatory chemical signals (cytokines) such as tumor necrosis factor-, interleukin-1, interleukin-6, and interleukin-22.[26] These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate.[26] One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10.[26]

Gene mutations of proteins involved in the skin's ability to function as a barrier have been identified as markers of susceptibility for the development of psoriasis.[41][42]

DNA released from dying cells acts as an inflammatory stimulus in psoriasis[43] and stimulates the receptors on certain dendritic cells, which in turn produce the cytokine interferon-.[43] In response to these chemical messages from dendritic cells and T cells, keratinocytes also secrete cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-, which signal downstream inflammatory cells to arrive and stimulate additional inflammation.[26]

Dendritic cells bridge the innate immune system and adaptive immune system. They are increased in psoriatic lesions[39] and induce the proliferation of T cells and type 1 helper T cells (Th1). Targeted immunotherapy as well as psoralen and ultraviolet A (PUVA) therapy can reduce the number of dendritic cells and favors a Th2 cell cytokine secretion pattern over a Th1/Th17 cell cytokine profile.[26][34] Psoriatic T cells move from the dermis into the epidermis and secrete interferon- and interleukin-17.[44] Interleukin-23 is known to induce the production of interleukin-17 and interleukin-22.[39][44] Interleukin-22 works in combination with interleukin-17 to induce keratinocytes to secrete neutrophil-attracting cytokines.[44]

A diagnosis of psoriasis is usually based on the appearance of the skin. Skin characteristics typical for psoriasis are scaly, erythematous plaques, papules, or patches of skin that may be painful and itch.[15] No special blood tests or diagnostic procedures are needed to make the diagnosis.[12][45]

The differential diagnosis of psoriasis includes dermatological conditions similar in appearance such as discoid eczema, seborrhoeic eczema, pityriasis rosea (may be confused with guttate psoriasis), nail fungus (may be confused with nail psoriasis) or cutaneous T cell lymphoma (50% of individuals with this cancer are initially misdiagnosed with psoriasis).[38] Dermatologic manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis.[38]

If the clinical diagnosis is uncertain, a skin biopsy or scraping may be performed to rule out other disorders and to confirm the diagnosis. Skin from a biopsy will show clubbed epidermal projections that interdigitate with dermis on microscopy. Epidermal thickening is another characteristic histologic finding of psoriasis lesions.[12][46] The stratum granulosum layer of the epidermis is often missing or significantly decreased in psoriatic lesions; the skin cells from the most superficial layer of skin are also abnormally as they never fully mature. Unlike their mature counterparts, these superficial cells keep their nucleus.[12] Inflammatory infiltrates can typically be visualized on microscopy when examining skin tissue or joint tissue affected by psoriasis. Epidermal skin tissue affected by psoriatic inflammation often has many CD8+ T cells while a predominance of CD4+ T cells make up the inflammatory infiltrates of the dermal layer of skin and the joints.[12]

Psoriasis is classified as a papulosquamous disorder and is most commonly subdivided into different categories based on histological characteristics.[2][5] Variants include plaque, pustular, guttate, and flexural psoriasis. Each form has a dedicated ICD-10 code.[47] Psoriasis can also be classified into nonpustular and pustular types.[48]

Another classification scheme considers genetic and demographic factors. Type 1 has a positive family history, starts before the age of 40, and is associated with the human leukocyte antigen, HLA-Cw6. Conversely, type 2 does not show a family history, presents before age 40, and is not associated with HLA-Cw6.[49] Type 1 accounts for about 75% of persons with psoriasis.[50]

The classification of psoriasis as an autoimmune disease has sparked considerable debate. Researchers have proposed differing descriptions of psoriasis and psoriatic arthritis; some authors have classified them as autoimmune diseases[12][27][51] while others have classified them as distinct from autoimmune diseases and referred to them as immune-mediated inflammatory diseases.[26][52][53]

There is no consensus about how to classify the severity of psoriasis. Mild psoriasis has been defined as a percentage of body surface area (BSA)10, a Psoriasis Area Severity Index (PASI) score 10, and a dermatology life quality index (DLQI) score 10.[54] Moderate to severe psoriasis was defined by the same group as BSA >10 or PASI score >10 and a DLQI score >10.[54] The DLQI is a 10 question tool used to measure the impact of several dermatologic diseases on daily functioning. The DLQI score ranges from 0 (minimal impairment) to 30 (maximal impairment) and is calculated with each answer being assigned 0-3 points with higher scores indicating greater social or occupational impairment.[55]

The psoriasis area severity index (PASI) is the most widely used measurement tool for psoriasis. PASI assesses the severity of lesions and the area affected and combines these two factors into a single score from 0 (no disease) to 72 (maximal disease).[56] Nevertheless, the PASI can be too unwieldy to use outside of research settings, which has led to attempts to simplify the index for clinical use.[57]

While no cure is available for psoriasis,[38] many treatment options exist. Topical agents are typically used for mild disease, phototherapy for moderate disease, and systemic agents for severe disease.[58]

Topical corticosteroid preparations are the most effective agents when used continuously for 8 weeks; retinoids and coal tar were found to be of limited benefit and may be no better than placebo.[59] Greater benefit has been observed with very potent corticosteroids when compared to potent corticosteroids. Vitamin D analogues such as paricalcitol were found to be significantly superior to placebo. Combination therapy with vitamin D and a corticosteroid was superior to either treatment alone and vitamin D was found to be superior to coal tar for chronic plaque psoriasis.[60]

Moisturizers and emollients such as mineral oil, petroleum jelly, calcipotriol, and decubal (an oil-in-water emollient) were found to increase the clearance of psoriatic plaques. Emollients have been shown to be even more effective at clearing psoriatic plaques when combined with phototherapy.[61] However, certain emollients have no impact on psoriasis plaque clearance or may even decrease the clearance achieved with phototherapy. The emollient salicylic acid is structurally similar to para-aminobenzoic acid (PABA), commonly found in sunscreen, and is known to interfere with phototherapy in psoriasis. Coconut oil, when used as an emollient in psoriasis, has been found to decrease plaque clearance with phototherapy.[61] Medicated creams and ointments applied directly to psoriatic plaques can help reduce inflammation, remove built-up scale, reduce skin turnover, and clear affected skin of plaques. Ointment and creams containing coal tar, dithranol, corticosteroids (i.e. desoximetasone), fluocinonide, vitamin D3 analogs (for example, calcipotriol), and retinoids are routinely used. The use of the finger tip unit may be helpful in guiding how much topical treatment to use.[30][62]

Vitamin D analogues may be useful with steroids; however, alone have a higher rate of side effects.[63] They may allow less steroids to be used.[64]

Another topical therapy used to treat psoriasis is a form of balneotherapy, which involves daily baths in the Dead Sea. This is usually done for four weeks with the benefit attributed to sun exposure. This is cost-effective and it has been propagated as an effective way to treat psoriasis without medication.[65] Decreases of PASI scores greater than 75% and remission for several months have commonly been observed.[65] Side-effects may be mild such as itchiness, folliculitis, sunburn, poikiloderma, and a theoretical risk of nonmelanoma skin cancer or melanoma has been suggested.[65] However, more recent studies have determined that there does not appear to be increased risk of melanoma in the long-term.[66] Data are inconclusive with respect to nonmelanoma skin cancer risk, but support the idea that the therapy is associated with an increased risk of benign forms of sun-induced skin damage such as, but not limited to, actinic elastosis or liver spots.[66] Dead Sea balneotherapy is also effective for psoriatic arthritis.[66]

Phototherapy in the form of sunlight has long been used for psoriasis.[58]Wavelengths of 311313nanometers are most effective, and special lamps have been developed for this application.[58] The exposure time should be controlled to avoid over exposure and burning of the skin. The UVB lamps should have a timer that will turn off the lamp when the time ends. The amount of light used is determined by a person's skin type.[58] Increased rates of cancer from treatment appear to be small.[58] Narrow band UVB light (NBUVB) phototherapy has been demonstrated to have similar efficacy to PUVA.[67]

A major mechanism of NBUVB is the induction of DNA damage in the form of pyrimidine dimers. This type of phototherapy is useful in the treatment of psoriasis because the formation of these dimers interferes with the cell cycle and stops it. The interruption of the cell cycle induced by NBUVB opposes the characteristic rapid division of skin cells seen in psoriasis.[67] The activity of many types of immune cells found in the skin is also effectively suppressed by NBUVB phototherapy treatments. The most common short-term side effect of this form of phototherapy is redness of the skin; less common side effects of NBUVB phototherapy are itching and blistering of the treated skin, irritation of the eyes in the form of conjunctival inflammation or inflammation of the cornea, or cold sores due to reactivation of the herpes simplex virus in the skin surrounding the lips. Eye protection is usually given during phototherapy treatments.[67]

Psoralen and ultraviolet A phototherapy (PUVA) combines the oral or topical administration of psoralen with exposure to ultraviolet A (UVA) light. The mechanism of action of PUVA is unknown, but probably involves activation of psoralen by UVA light, which inhibits the abnormally rapid production of the cells in psoriatic skin. There are multiple mechanisms of action associated with PUVA, including effects on the skin's immune system. PUVA is associated with nausea, headache, fatigue, burning, and itching. Long-term treatment is associated with squamous cell carcinoma (but not with melanoma).[31][68] A combination therapy for moderate to severe psoriasis using PUVA plus acitretin resulted in benefit, but acitretin use has been associated with birth defects and liver damage.[69]

Psoriasis resistant to topical treatment and phototherapy may be treated with systemic therapies including oral medications or injectable treatments.[70] Patients undergoing systemic treatment must have regular blood and liver function tests to check for medication toxicities.[70]Pregnancy must be avoided for most of these treatments. The majority of people experience a recurrence of psoriasis after systemic treatment is discontinued.

Non-biologic systemic treatments frequently used for psoriasis include methotrexate, ciclosporin, hydroxycarbamide, fumarates such as dimethyl fumarate, and retinoids.[71] Methotrexate and ciclosporin are drugs that suppress the immune system; retinoids are synthetic forms of vitamin A. These agents are also regarded as first-line treatments for psoriatic erythroderma.[9]

Biologics are manufactured proteins that interrupt the immune process involved in psoriasis. Unlike generalised immunosuppressive drug therapies such as methotrexate, biologics target specific aspects of the immune system contributing to psoriasis.[71] These medications are generally well-tolerated and limited long-term outcome data have demonstrated biologics to be safe for long-term use in moderate to severe plaque psoriasis.[71][72] However, due to their immunosuppressive actions, biologics have been associated with a small increase in the risk for infection.[71] Professional guidelines regard biologics as third-line treatment for plaque psoriasis following inadequate response to topical treatment, phototherapy, and non-biologic systemic treatments.[72] The safety of biologics during pregnancy has not been assessed. European guidelines recommend avoiding biologics if a pregnancy is planned; anti-TNF therapies such as infliximab are not recommended for use in chronic carriers of the hepatitis B virus or individuals infected with HIV.[71]

Several monoclonal antibodies target cytokines, the molecules that cells use to send inflammatory signals to each other. TNF- is one of the main executor inflammatory cytokines. Four monoclonal antibodies (MAbs) (infliximab, adalimumab, golimumab, and certolizumab pegol) and one recombinant TNF- decoy receptor, etanercept, have been developed to inhibit TNF- signaling. Additional monoclonal antibodies have been developed against pro-inflammatory cytokines interleukin-12, interleukin-23 and interleukin-17[73] and inhibit the inflammatory pathway at a different point than the anti-TNF- antibodies.[26] IL-12 and IL-23 share a common domain, p40, which is the target of the recently FDA-approved ustekinumab.[27]

Two drugs that target T cells are efalizumab and alefacept. Efalizumab is a monoclonal antibody that specifically targets the CD11a subunit of LFA-1.[71] It also blocks the adhesion molecules on the endothelial cells that line blood vessels, which attract T cells. Efalizumab was voluntarily withdrawn from the European market in February 2009 and from the US market in June 2009 by the manufacturer due to the medication's association with cases of progressive multifocal leukoencephalopathy.[71] Alefacept also blocks the molecules that dendritic cells use to communicate with T cells and even causes natural killer cells to kill T cells as a way of controlling inflammation.[26]

Individuals with psoriasis may develop neutralizing antibodies against monoclonal antibodies. Neutralization occurs when an antidrug antibody prevents a monoclonal antibody such as infliximab from binding antigen in a laboratory test. Specifically, neutralization occurs when the antidrug antibody binds to infliximab's antigen binding site instead of TNF-. When infliximab no longer binds tumor necrosis factor alpha, it no longer decreases inflammation, and the psoriasis may worsen. Neutralizing antibodies have not been reported against etanercept, a biologic-drug that is a fusion protein composed of two TNF- receptors. The lack of neutralizing antibodies against etanercept is probably secondary to the innate presence of the TNF- receptor, and the development of immune tolerance.[74]

Limited evidence suggests removal of the tonsils may benefit people with chronic plaque psoriasis, guttate psoriasis, and palmoplantar pustulosis.[75][76]

Uncontrolled studies have suggested that individuals with psoriasis or psoriatic arthritis may benefit from a diet supplemented with fish oil rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).[77] Conflicting evidence exists indicating that there may be an increased incidence of psoriasis in people with celiac disease. Psoriatic disease severity decreased after 3 months of a gluten free diet in patients with anti-gliadin antibodies.[77]

Most people with psoriasis experience nothing more than mild skin lesions that can be treated effectively with topical therapies.[59]

Psoriasis is known to have a negative impact on the quality of life of both the affected person and the individual's family members.[27] Depending on the severity and location of outbreaks, individuals may experience significant physical discomfort and some disability. Itching and pain can interfere with basic functions, such as self-care and sleep.[40] Participation in sporting activities, certain occupations, and caring for family members can become difficult activities for those with plaques located on their hands and feet.[40] Plaques on the scalp can be particularly embarrassing, as flaky plaque in the hair can be mistaken for dandruff.[78]

Individuals with psoriasis may feel self-conscious about their appearance and have a poor self-image that stems from fear of public rejection and psychosexual concerns. Psoriasis has been associated with low self-esteem and depression is more common among those with the condition.[2] People with psoriasis often feel prejudiced against due to the commonly held incorrect belief that psoriasis is contagious.[40] Psychological distress can lead to significant depression and social isolation; a high rate of thoughts about suicide has been associated with psoriasis.[17] Many tools exist to measure the quality of life of patients with psoriasis and other dermatological disorders. Clinical research has indicated individuals often experience a diminished quality of life.[79] Children with psoriasis may encounter bullying.[80]

Several conditions are associated with psoriasis. These occur more frequently in older people. Nearly half of individuals with psoriasis over the age of 65 have at least three comorbidities, and two-thirds have at least two comorbidities.[81]

Psoriasis has been associated with obesity[2] and several other cardiovascular and metabolic disturbances. The incidence of diabetes is 27% higher in people affected by psoriasis than in those without the condition.[82] Severe psoriasis may be even more strongly associated with the development of diabetes than mild psoriasis.[82] Younger people with psoriasis may also be at increased risk for developing diabetes.[81][83] Individuals with psoriasis or psoriatic arthritis have a slightly higher risk of heart disease and heart attacks when compared to the general population. Cardiovascular disease risk appeared to be correlated with the severity of psoriasis and its duration. There is no strong evidence to suggest that psoriasis is associated with an increased risk of death from cardiovascular events. Methotrexate may provide a degree of protection for the heart.[31][81]

The odds of having hypertension are 1.58 times higher in people with psoriasis than those without the condition; these odds are even higher with severe cases of psoriasis. A similar association was noted in people who have psoriatic arthritisthe odds of having hypertension were found to be 2.07 times greater when compared to odds of the general population. The link between psoriasis and hypertension is not currently understood. Mechanisms hypothesized to be involved in this relationship include the following: dysregulation of the renin-angiotensin system, elevated levels of endothelin 1 in the blood, and increased oxidative stress.[83][84] The incidence of the heart rhythm abnormality atrial fibrillation is 1.31 times higher in people with mild psoriasis and 1.63 times higher in people with severe psoriasis.[85] There may be a slightly increased risk of stroke associated with psoriasis, especially in severe cases.[31][86] Treating high levels of cholesterol with statins has been associated with decreased psoriasis severity, as measured by PASI score, and has also been associated with improvements in other cardiovascular disease risk factors such as markers of inflammation.[87] These cardioprotective effects are attributed to ability of statins to improve blood lipid profile and because of their anti-inflammatory effects. Statin use in those with psoriasis and hyperlipidemia was associated with decreased levels of high-sensitivity C-reactive protein and TNF as well as decreased activity of the immune protein LFA-1.[87] Compared to individuals without psoriasis, those affected by psoriasis are more likely to satisfy the criteria for metabolic syndrome.[12][85]

The rates of Crohn's disease and ulcerative colitis are increased when compared with the general population, by a factor of 3.8 and 7.5 respectively.[2] Few studies have evaluated the association of multiple sclerosis with psoriasis, and the relationship has been questioned.[2][88] Psoriasis has been associated with a 16% increase in overall relative risk for non-skin cancer.[31] People with psoriasis have a 52% increased risk cancers of the lung and bronchus, a 205% increase in the risk of developing cancers of the upper gastrointestinal tract, a 31% increase in the risk of developing cancers of the urinary tract, a 90% increase in the risk of developing liver cancer, and a 46% increase in the risk of developing pancreatic cancer.[31] The risk for development of non-melanoma skin cancers is also increased. Psoriasis increases the risk of developing squamous cell carcinoma of the skin by 431% and increases the risk of basal cell carcinoma by 100%.[31] There is no increased risk of melanoma associated with psoriasis.[31]

Psoriasis is estimated to affect 2-4% of the population of the western world.[6] The rate of psoriasis varies according to age, gender, region and ethnicity; a combination of environmental and genetic factors is thought to be responsible for these differences.[6] It can occur at any age, although it most commonly appears for the first time between the ages of 15 and 25 years. Approximately one third of psoriasis patients report being diagnosed before age 20.[89] Psoriasis affects both sexes equally.[49]

People with inflammatory bowel disease such as Crohn's disease or ulcerative colitis are at an increased risk of developing psoriasis.[37] Psoriasis is more common in countries farther from the equator.[37] Persons of white European ancestry are more likely to have psoriasis and the condition is relatively uncommon in African Americans and extremely uncommon in Native Americans.[38]

Scholars believe psoriasis to have been included among the various skin conditions called tzaraath (translated as leprosy) in the Hebrew Bible, a condition imposed as a punishment for slander. The patient was deemed "impure" (see tumah and taharah) during their afflicted phase and is ultimately treated by the kohen.[90] However, it is more likely that this confusion arose from the use of the same Greek term for both conditions. The Greeks used the term lepra () for scaly skin conditions. They used the term psora to describe itchy skin conditions.[90] It became known as Willan's lepra in the late 18th century when English dermatologists Robert Willan and Thomas Bateman differentiated it from other skin diseases. Leprosy, they said, is distinguished by the regular, circular form of patches, while psoriasis is always irregular. Willan identified two categories: leprosa graecorum and psora leprosa.[91]

Psoriasis is thought to have first been described in Ancient Rome by Cornelius Celsus. The disease was first classified by English physician Thomas Willan. The British dermatologist Thomas Bateman described a possible link between psoriasis and arthritic symptoms in 1813.[92]

The history of psoriasis is littered with treatments of dubious effectiveness and high toxicity. In the 18th and 19th centuries, Fowler's solution, which contains a poisonous and carcinogenic arsenic compound, was used by dermatologists as a treatment for psoriasis.[90]Mercury was also used for psoriasis treatment during this time period.[90]Sulfur, iodine, phenol were also commonly used treatments for psoriasis during this era when it was incorrectly believed that psoriasis was an infectious disease.[90] Coal tars were widely used with ultraviolet light irradiation as a topical treatment approach in the early 1900s.[90][93] During the same time period, psoriatic arthritis cases were treated with intravenously administered gold preparations in the same manner as rheumatoid arthritis.[93] All of these treatments have been replaced with modern topical and systemic therapies.

The word psoriasis is from Greek , meaning "itching condition" or "being itchy"[94] from psora, "itch" and -iasis, "action, condition".

The International Federation of Psoriasis Associations (IFPA) is the global umbrella organization for national and regional psoriasis patient associations and also gathers the leading experts in psoriasis and psoriatic arthritis research for scientific conferences every three years.[95] The Psoriasis International Network, a program of the Fondation Ren Touraine, gathers dermatologists, rheumatologists and other caregivers involved in the management of psoriasis. Non-profit organizations the National Psoriasis Foundation in the United States, the Psoriasis Association in the United Kingdom, and Psoriasis Australia offer advocacy and education about psoriasis in their respective countries.

Psoriasis is a skin disease that causes itchy or sore patches of thick, red skin with silvery scales. You usually get the patches on your elbows, knees, scalp, back, face, palms and feet, but they can show up on other parts of your body. Some people who have psoriasis also get a form of arthritis called psoriatic arthritis.

A problem with your immune system causes psoriasis. In a process called cell turnover, skin cells that grow deep in your skin rise to the surface. Normally, this takes a month. In psoriasis, it happens in just days because your cells rise too fast.

Psoriasis can be hard to diagnose because it can look like other skin diseases. Your doctor might need to look at a small skin sample under a microscope.

Psoriasis can last a long time, even a lifetime. Symptoms come and go. Things that make them worse include

Psoriasis usually occurs in adults. It sometimes runs in families. Treatments include creams, medicines, and light therapy.

NIH: National Institute of Arthritis and Musculoskeletal and Skin Diseases

These patches normally appear on your elbows, knees, scalp and lower back, but can appear anywhere on your body.Most people are only affected with small patches. In some cases, the patches can be itchy or sore.

Psoriasis affects around 2% of people in the UK. It can start at any age, but most often develops in adults under 35 years old. The condition affects men and women equally.

The severity of psoriasis varies greatly from person to person. For some people it's just a minor irritation, but for others it can havea major impact on their quality of life.

Psoriasis is a long-lasting (chronic) disease that usually involves periods when you have no symptoms ormild symptoms, followed by periods when symptoms are more severe.

Read more about the symptoms of psoriasis.

People with psoriasis have anincreased production of skin cells.

Skin cells are normallymade and replaced every three to four weeks, but in psoriasis this process only lasts about three to seven days. The resulting build-up of skin cells is what creates the patches associated with psoriasis.

Although the process isn't fully understood, it's thoughtto be related to a problem with the immune system. The immune systemis your body's defence against disease and infection, but for people with psoriasis, it attacks healthy skin cells by mistake.

Psoriasis can run in families,although the exact role that genetics plays in causing psoriasis is unclear.

It typically affects the outside of the elbows, knees or scalp, though it can appear on any location. Some people report that psoriasis is itchy, burns and stings. Psoriasis is associated with other serious health conditions, such as diabetes, heart disease and depression.

If you develop a rash that doesn't go away with an over-the-counter medication, you should consider contacting your doctor.

While scientists do not know what exactly causes psoriasis, we do know that the immune system and genetics play major roles in its development. Usually, something triggers psoriasis to flare. The skin cells in people with psoriasis grow at an abnormally fast rate, which causes the buildup of psoriasis lesions.

Men and women develop psoriasis at equal rates. Psoriasis also occurs in all racial groups, but at varying rates. About 1.3 percent of African-Americans have psoriasis, compared to 2.5 percent of Caucasians.

Psoriasis often develops between the ages of 15 and 35, but it can develop at any age. About 10 to 15 percent of those with psoriasis get it before age 10. Some infants have psoriasis, although this is considered rare.

Psoriasis is not contagious. It is not something you can "catch" or that others can catch from you. Psoriasis lesions are not infectious.

There are no special blood tests or tools to diagnose psoriasis. A dermatologist (doctor who specializes in skin diseases) or other health care provider usually examines the affected skin and determines if it is psoriasis.

Your doctor may take a piece of the affected skin (a biopsy) and examine it under the microscope. When biopsied, psoriasis skin looks thicker and inflamed when compared to skin with eczema.

Your doctor also will want to learn about your family history. About one-third of people with psoriasis have a family member with the disease, according to dermatologist Dr. Paul Yamauchi with the Dermatology and Skin Care Institute in Santa Monica, Calif.

There are five types of psoriasis. Learning more about your type of psoriasis will help you determine the best treatment for you.

This publication contains general information about psoriasis. It describes what psoriasis is, what causes it, and what the treatment options are. If you have further questions after reading this publication, you may wish to discuss them with your doctor.

Psoriasis is a chronic (long-lasting) skin disease of scaling and inflammation that affects greater than 3 percent of the U.S. population, or more than 5 million adults. Although the disease occurs in all age groups, it primarily affects adults. It appears about equally in males and females.

Psoriasis occurs when skin cells quickly rise from their origin below the surface of the skin and pile up on the surface before they have a chance to mature. Usually this movement (also called turnover) takes about a month, but in psoriasis it may occur in only a few days.

In its typical form, psoriasis results in patches of thick, red (inflamed) skin covered with silvery scales. These patches, which are sometimes referred to as plaques, usually itch or feel sore. They most often occur on the elbows, knees, other parts of the legs, scalp, lower back, face, palms, and soles of the feet, but they can occur on skin anywhere on the body. The disease may also affect the fingernails, the toenails, and the soft tissues of the genitals, and inside the mouth. Although it is not unusual for the skin around affected joints to crack, some people with psoriasis experience joint inflammation that produces symptoms of arthritis. This condition is called psoriatic arthritis.

Individuals with psoriasis may experience significant physical discomfort and some disability. Itching and pain can interfere with basic functions, such as self-care, walking, and sleep. Plaques on hands and feet can prevent individuals from working at certain occupations, playing some sports, and caring for family members or a home. The frequency of medical care is costly and can interfere with an employment or school schedule. People with moderate to severe psoriasis may feel self-conscious about their appearance and have a poor self-image that stems from fear of public rejection and concerns about intimate relationships. Psychological distress can lead to significant depression and social isolation.

Psoriasis is a skin disorder driven by the immune system, especially involving a type of white blood cell called a T cell. Normally, T cells help protect the body against infection and disease. In the case of psoriasis, T cells are put into action by mistake and become so active that they trigger other immune responses, which lead to inflammation and to rapid turnover of skin cells.

In many cases, there is a family history of psoriasis. Researchers have studied a large number of families affected by psoriasis and identified genes linked to the disease. Genes govern every bodily function and determine the inherited traits passed from parent to child.

People with psoriasis may notice that there are times when their skin worsens, called flares, then improves. Conditions that may cause flares include infections, stress, and changes in climate that dry the skin. Also, certain medicines, including beta-blockers, which are prescribed for high blood pressure, and lithium may trigger an outbreak or worsen the disease. Sometimes people who have psoriasis notice that lesions will appear where the skin has experienced trauma. The trauma could be from a cut, scratch, sunburn, or infection.

Occasionally, doctors may find it difficult to diagnose psoriasis, because it often looks like other skin diseases. It may be necessary to confirm a diagnosis by examining a small skin sample under a microscope.

Pityriasis rosea (also known as pityriasis rosea Gibert[1]) is a skin rash. It is benign but may inflict substantial discomfort in certain cases.[2] Classically, it begins with a single "herald patch" lesion, followed in 1 or 2 weeks by a generalized body rash lasting up to 12 weeks, however usually around 6 - 8.[3][4][5]

The symptoms of this condition include:

The cause of pityriasis rosea is not certain, but its clinical presentation and immunologic reactions suggest a viral infection as a cause. Some believe it to be a reactivation of herpes viruses 6 and 7, which cause roseola in infants.[9][10][11][12]

Experienced practitioners may make the diagnosis clinically.[5] If the diagnosis is in doubt, tests may be performed to rule out similar conditions such as Lyme disease, ringworm, guttate psoriasis, nummular or discoid eczema, drug eruptions, other viral exanthems.[5][13] A biopsy of the lesions will show extravasated erythrocytes within dermal papillae and dyskeratotic cells within the dermis.[5]

A set of validated diagnostic criteria for pityriasis rosea[14][15] is as follows: